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Fig. 5. Loss of Fgf8 specifically disrupts the Isl1/Mef2c pathway in the
AHF. In situ hybridized embryos; genotypes listed at the top, riboprobe
and somite stage at the left. (A) Mef2c in 10ss embryos; right
lateral view, red arrowheads indicate decreased signal in the OFT and AHF/SM
of mutants. (A') Dorsal views; the ring of staining around the
nascent OFT is markedly less intense in the mutants (red arrowheads).
(B,B') Wnt11 at 20-21ss; close up of right side
of the heart. Note the undetectable signal in the OFT myocardium of severe
mutants (red arrowheads), and decreased levels in the mild variants (B');
expression is intact in Fgf8C/-;Mef2cAHFCre mutants (black
arrowhead). (C-C'') Pitx2 at 15ss; right lateral views in
C, transverse sections in C',C''. Upper panels are at the level of
the OFT, lower panels at level of the atrium/sinus venosus.
(D,D') Tbx1 expression in transverse-sectioned
9-10ss embryos appears normal in the endoderm and SM/AHF.
(E,E') Fgf10 in transverse-sectioned 8ss embryos.
Expression is intact (black arowheads) except in mutant proximal OFT
myocardium (red arrowheads).
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